ArticleThe Journal of experimental medicine1993
Mycobacterial virulence. Virulent strains of Mycobacteria tuberculosis have faster in vivo doubling times and are better equipped to resist growth-inhibiting functions of macrophages in the presence and absence of specific immunity.
Article in The Journal of experimental medicine, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 138 citations in OpenAlex.
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- Quantitative proteomics reveals that dormancy-related proteins mediate the attenuation in mycobacterium strains.Virulence · 2021Article
- HDAC3 inhibitor RGFP966 controls bacterial growth and modulates macrophage signaling during Mycobacterium tuberculosis infection.Tuberculosis (Edinburgh, Scotland) · 2021Article
- Putative determinants of virulence inVirulence · 2020Article
- Artemisia annua and Artemisia afra extracts exhibit strong bactericidal activity against Mycobacterium tuberculosis.Journal of ethnopharmacology · 2020Article
- Capsular glycan recognition provides antibody-mediated immunity against tuberculosis.The Journal of clinical investigation · 2020Article
- Article
- Humanized NOG mice as a model for tuberculosis vaccine-induced immunity: a comparative analysis with the mouse and guinea pig models of tuberculosis.Immunology · 2017Article
- Optimisation of a murine splenocyte mycobacterial growth inhibition assay using virulent Mycobacterium tuberculosis.Scientific reports · 2017Article
- A Mutation in the 16S rRNA Decoding Region Attenuates the Virulence of Mycobacterium tuberculosis.Infection and immunity · 2016Article
- Development of an Intracellular Screen for New Compounds Able To Inhibit Mycobacterium tuberculosis Growth in Human Macrophages.Antimicrobial agents and chemotherapy · 2016Article
- Bacillary replication and macrophage necrosis are determinants of neutrophil recruitment in tuberculosis.Microbes and infection · 2015Article
- Review of the prevalence and drug resistance of tuberculosis in prisons: a hidden epidemic.Epidemiology and infection · 2015Review
- Evolution of M. bovis BCG Vaccine: Is Niacin Production Still a Valid Biomarker?Tuberculosis research and treatment · 2015Review
- Evolutionary history of tuberculosis shaped by conserved mutations in the PhoPR virulence regulator.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Effects of P-MAPA Immunomodulator on Toll-Like Receptors and p53: Potential Therapeutic Strategies for Infectious Diseases and Cancer.Infectious agents and cancer · 2012Article
- Complete annotated genome sequence of Mycobacterium tuberculosis Erdman.Journal of bacteriology · 2012Article
- Epidemiologic consequences of microvariation in Mycobacterium tuberculosis.The Journal of infectious diseases · 2012Article
- Comparative studies evaluating mouse models used for efficacy testing of experimental drugs against Mycobacterium tuberculosis.Antimicrobial agents and chemotherapy · 2011Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The kinetics of growth of two virulent strains of mycobacteria (M. tuberculosis Erdman and M. tuberculosis H37Rv) and two attenuated strains (M. tuberculosis H37Ra and M. bovis Bacillus Calmette-Guerin [BCG]) were studied in the lungs, livers, spleens, and kidneys of severe combined immunodeficient (SCID) mice and of their coisogenic CB-17 immunocompetent counterparts. It was found, in keeping with the findings of earlier investigators (Pierce, C. H., R. J. Dubos, and W. B. Schaefer. 1953. J. Exp. Med. 97:189.), that in immunocompetent mice, virulent organisms grew progressively only in the lungs, whereas the growth of attenuated organisms was controlled in all organs. In SCID mice, in contrast, virulent mycobacteria grew rapidly and progressively in all organs, as did BCG, although at a slower rate. However, H37Ra failed to grow progressively in any organs of SCID mice, unless the mice were treated with hydrocortisone. In fact, hydrocortisone treatment enabled virulent, as well as attenuated, organisms to grow strikingly more rapidly in all organs of SCID mice and in all organs of CB-17 mice. A histological study showed that in SCID mice, multiplication of mycobacteria in the liver occurs in the cytoplasm of macrophages in granulomas and presumably in macrophages in other organs. It is suggested, therefore, that the macrophages of SCID mice possess a glucocorticoid-sensitive mycobacterial mechanism that prevents virulent and avirulent mycobacteria from expressing their true minimal doubling times. In the absence of this mechanism in the lungs of hydrocortisone-treated SCID mice, the doubling times of Erdman, H37Rv, BCG, and H37Ra were 17.7, 17.4, 44.6, and 98.6 h, respectively. The possible importance of a rapid multiplication rate for mycobacterial virulence is discussed.
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